Let-7c inhibition conversely decreased paclitaxel-induced apoptosis. It is known that let-7a microRNA, a member of the let-7 family, inhibits growth of endometrial carcinoma cells targeting Aurora-B that controls progression through each phase of mitosis. We thus studied whether let-7c mediates Aurora-B expression in ESC cells. The expression levels of Aurora-B mRNA and protein were higher in USPC-PTXR1 cells compared with USPC1 cells. Let-7c inhibition increased Aurora-B expression in USPC1 cells but decreased Aurora-B expression in USPC1-PTXR1 cells. These results indicate that let-7c mediates paclitaxel resistance via inhibition of Aurora-B expression in ESC cells.Reports on an association between body mass index and aortic disease, which remains controversial. This study investigated the association between body mass index and mortality from aortic disease.
We conducted the Japan Collaborative Cohort Study, a prospective study of 103,972 Japanese men and women aged 40-79 years. Body mass index was calculated on the basis of self-reported height and weight, and the participants were followed up from 1988-89 through 2009. Sex-specific hazard ratios (95% confidence intervals) of mortality from aortic disease according to quintiles of body mass index were analyzed using the Cox proportional hazards model.
During the median 18.8 years of follow-up, we documented 139 deaths due to aortic aneurysm (including 51 thoracic and 74 abdominal aortic aneurysms) and 134 deaths due to aortic dissection. We observed positive associations of body mass index with mortality from aortic aneurysm among men the multivariable hazard ratios (95% confidence intervals) for highest versus lowest quintiles of body mass index were 4.48 (2.10- 9.58), P for trend ＜0.0001 for aortic aneurysm; 6.52 (1.33-32.02), P=0.005 for thoracic aortic aneurysm; 3.81 (1.39-10.49), P=0.01 for abdominal aortic aneurysm; and 2.71 (1.59-4.62), P=0.001 for total aortic disease. No association was found for aortic dissection. Among ever-smokers (men ? 90%) but not never-smokers (women ? 84%), an association between body mass index and aortic disease mortality was observed regardless of sex, which may explain the sex difference (P for sex-interaction=0.046).
We found a positive association between body mass index and mortality from aortic aneurysm among Japanese men and smokers.
We found a positive association between body mass index and mortality from aortic aneurysm among Japanese men and smokers.Calreticulin (CRT) and calnexin (CNX), homologous major chaperones in the endoplasmic reticulum (ER), are known to translocate to the cell surface in response to chemotherapeutic agents, such as mitoxantrone (MIT), and cellular stresses, including apoptosis. Cell surface CRT (ecto-CRT) is relevant to the phagocytic uptake of cancer cells and dying cells, and pre-apoptotic exposure of CRT has been reported to result in enhanced immunogenicity of dying tumor cells, serving as a damage-associated molecular pattern (DAMP). In this study, HT-29 cells were treated with MIT to induce ER stress, and ecto-CRT and cell surface CNX were quantified by flow cytometry in the absence or presence of caspase inhibitors, a calpain inhibitor, or a scavenger of reactive oxygen species. https://www.selleckchem.com/products/hc-7366.html The biphasic (early transient and late sustained) increase of ecto-CRT on HT-29 cells was observed after treatment with MIT. We confirmed that the early increase in ecto-CRT after 4?h of MIT treatment was not related to apoptosis, whereas the increase of ecto-CRT, as well as that of cell-surface CNX, during the later stage of treatment was caspase dependent and related to apoptosis. In addition, our results suggested that the early peak of ecto-CRT was mediated by activation of caspase 8 by ER stress. Thus, the physiological significance of the late increases in cell-surface CRT and/or CNX might be considered an "eat-me signal" for the removal of dead cells by phagocytosis, while the early increase in ecto-CRT caused by ER stress might enhance the immunogenicity of stressed tumor cells.Entoloma sarcopum is widely known as an edible mushroom but appears morphologically similar to the poisonous mushrooms E. rhodopolium sensu lato (s. l.) and E. sinuatum s. l. Many cases of food poisoning caused by eating these poisonous mushrooms occur each year in Japan. Therefore, they were recently reclassified based on both morphological and molecular characteristics as sensu stricto species. In this study, we analyzed the nucleotide sequences of the rRNA gene (rDNA) cluster region, mainly including the internal transcribed spacer regions and mitochondrial cytochrome oxidase 1 (CO1) gene, in E. sarcopum and its related species, to evaluate performances of these genes as genetic markers for identification and molecular phylogenetic analysis. We found that the CO1 gene contained lineage-specific insertion/deletion sequences, and our CO1 tree yielded phylogenetic information that was not supported by analysis of the rDNA cluster region sequence. Our results suggested that the CO1 gene is a better genetic marker than the rDNA cluster region, which is the most widely used marker for fungal identification and classification, for discrimination between edible and poisonous mushrooms among Japanese E. sarcopum and related species. Our study thus reports a new genetic marker that is useful for detection of Japanese poisonous mushrooms, Entoloma.Generally, the olfactory organ of vertebrates consists of the olfactory epithelium (OE) and the vomeronasal organ (VNO). The OE contains ciliated olfactory receptor neurons (ORNs), while the VNO contains microvillous ORNs. The ORNs in the OE express odorant receptors (ORs), while those in the VNO express type 1 and type 2 vomeronasal receptors (V1Rs and V2Rs). In turtles, the olfactory organ consists of the upper (UCE) and lower chamber epithelia (LCE). The UCE contains ciliated ORNs, while the LCE contains microvillous ORNs. Here we investigated the distribution of cells expressing vomeronasal receptors in the olfactory organ of turtles. The turtle vomeronasal receptors were encoded by two V1R genes and two V2R genes. Among them, V2R1 and V2R26 were mainly expressed in the LCE, while V1R3 was expressed both in the UCE and LCE. Notably, vomeronasal receptors were expressed by a limited number of ORNs, which was confirmed by the expression of the gene encoding TRPC2, an ion channel involved in the signal transduction of vomeronasal receptors.